急性冠脉综合症PCI时氯比格雷的合理应用.pptVIP

急性冠脉综合症PCI时氯比格雷合理应用 急性冠脉综合症机制 是急性心肌缺血引起的急性心肌事件。 主要以冠状动脉粥样硬化斑块破溃继发完全或不完全闭塞性血栓形成为病理基础。 急性冠脉综合症、经皮冠脉介入术后引发血栓形成关键因素 血小板激活、聚集 氯比格雷作用机制 限制二磷酸腺苷(ADP)与其血小板受体的结合及继发的ADP介导的糖蛋白GPlIb/HIa复合物的活化，因此可抑制血小板聚集。 阻断由释放的ADP引起的血小板活化的扩增，抑制其他激动剂诱导的血小板聚集 。 氯比格雷作用重要参数 为时间和剂量依赖型 达到最大血小板抑制效应： 负荷剂量300mg——2小时 75mg,qd——5天 连续给药3-7天血小板抑制作用达到稳态 停药5天后血小板凝聚、出血时间回归基线 Early and sustained dual oral antiplatelet therapy following percutaneous coronary intervention Patients were randomly assigned to receive a 300-mg clopidogrel loading dose (n = 1053) or placebo (n = 1063) 3 to 24 hours before PCI. Thereafter, all patients received clopidogrel, 75 mg/d, through day 28. From day 29 through 12 months, patients in the loading-dose group received clopidogrel, 75 mg/d, and those in the control group received placebo. Both groups received aspirin throughout the study. MAIN OUTCOME MEASURES: One-year incidence of the composite of death, myocardial infarction (MI), or stroke in the intent-to-treat population; 28-day incidence of the composite of death, MI, or urgent target vessel revascularization in the per-protocol population. RESULTS At 1 year, long-term clopidogrel therapy was associated with a 26.9% relative reduction in the combined risk of death, MI, or stroke (95% confidence interval [CI], 3.9%-44.4%; P =.02; absolute reduction, 3%). Clopidogrel pretreatment did not significantly reduce the combined risk of death, MI, or urgent target vessel revascularization at 28 days (reduction, 18.5%; 95% CI, -14.2% to 41.8%; P =.23). However, in a prespecified subgroup analysis, patients who received clopidogrel at least 6 hours before PCI experienced a relative risk reduction of 38.6% (95% CI, -1.6% to 62.9%; P =.051) for this end point compared with no reduction with treatment less than 6 hours before PCI. Risk of major bleeding at 1 year increased, but not significantly (8.8% with clopidogrel vs 6.7% with placebo; P =.07). CONCLUSIONS: Following PCI, long-term (1-year) clopidogr